Nursing Care of Patients with Hepatobiliary Disorders

Nursing Care of Patients with Hepatobiliary Disorders

Nursing Care of Patients with Hepatobiliary Disorders C. Cummings RN, EdD. Anatomy Diaphragm Liver Hepatic Duct

Cystic Duct Gall Bladder Common Bile Duct Pancreas Sphincter of Oddi

Duodenum Pancreas Exocrine- 80% of organ, acinar cells with digestive enzymes: What are they? Endocrine- islets of langerhans Alpha cells- ? Beta cells- ?

Acute Pancreatitis Cause: Pancreatic enzymes destroy ductal tissue and cancreatic cells autodigestion and fibrosis Can be life threatening NHP- necrotizing hemorrhagic pancreatitis 20%, diffuse bleeding Enzymes are activated before they reach the duodenum Toxic injury to pancreatic cells Four major physiologic processes

Lipolysis Caused by lipase, release fatty acids and combine with I Ca causes? Proteolysis Caused by trypsin, splits proteins into smaller polypeptides what?? Four major physiologic processes Necrosis of the Blood Vessels Caused by elastase, elastic fibers of the blood vessels and ducts dissolve what?

Kallikrein releases vasoactive peptides, bradykinin and kinin what? and increased ? Inflammation Leukocytes form around hemorrhagic and necrotic areas pus, abcess formation and if walled off pancreatic what?? Why does enzyme activation occur? Bile Reflux- obstruction of CBD Hypersecretion-obstruction theory- pancreatic duct ruptures Alcohol induced changes- stimulates hydrochloric

acid and secretin production exocrine functions, also causes edema of the duodenum and ampulla of Vater, this obstructs flow, may also decrease tone at sphincter of Oddi and cause duodenal reflux Other causes Besides alcohol ingestion and biliary disorders, can also be caused by: Trauma- blunt or surgical (whipple/ ERCP) Pancreatic obstruction- such as? Metabolic disturbances- hyperlipidemia,

hyperparathyroid Renal failure or transplant Ulcers that lead to peritonitis Coxsackievirus B infections Drug toxicities- such as? Complications

Pancreatic infection Peritonitis Hypovolemia Hemorrhage ARF Paralytic ileus

Septic Shock What are other complications?? Symptoms of Acute Pancreatitis What is predominant symptom? Where is it? When is it worse? Jaundice Cullens sign- what is that?

Turners sign- and that? Bowel sounds may be decreased or absent Abdominal tenderness Watch for signs of shock Respiratory effusions/ SOB Assess for excessive alcohol intake Turners sign

Laboratory Diagnoses Elevated Serum What are major enzymes? Trypsin

Elastase Also, increased serum Glucose Bilirubin Alanine aminotransferase Leukocyte count Decreased Calcium and magnesium Diagnoses for Acute Pancreatitis

What are two primary nursing diagnoses? Nausea Risk for fluid volume deficit Risk for infection Risk for ineffective breathing pattern

Risk for activity and sleep disturbances Collaborative Diagnoses What are two potential nursing diagnoses? Potential for Hypovolemic or Septic Shock

Potential for ARDS Potential for Paralytic Ileus Potential for MOSF Nursing Interventions Acute Pain What is primary method to relieve pain, other than medication? IV fluids for hydration

Replacement of Ca and Mg NG drainage and suction Assess for return of bowel sounds and pain control Pain Control Opiods, IV and PCA Demerol for relief of spasms at the sphincter of Oddi, but it has problems with breakdown and is rarely

used now Fentanyl patch Epidural morphine with bipivacaine Pain may last how long? Other management of pain Anticholinergics, atropine, glucagon, calcitonin, histamine receptor antagonists (Zantac), protease inhibitors are used for what?

Antibiotics Ceftazidime, cefuroxime, imipenem (Primaxin) Other Management of Pain Surgery ERCP (endoscopic retrograde cholangiopancreatography) - used to open sphincter Pseudocystojejunostomy or Pseudocystogastrotomy to drain abcess or pseudocyst

JP drains or sump tubes may be used for excessive drainage ERCP ERCP Imbalanced nutrition: less than body requirements

Maintain on NPO, may have NGT May not eat for 7-10 days Receive nutritional support through what? Begin back on what kind of diet? What should they not take in? Diet teaching and teaching on signs of chronic progression should be stressed with the patient

Chronic Pancreatitis Usually develops after repeated episodes of acute pancreatitis What is the most common cause? Types: Chronic Calcifying Pancreatitis- alcohol induced, proteins plug the ducts lead to atrophy and dilation ulceration and inflammation fibrosis, intraductal calification and cystic sacs

develop Hard, firm organ with pancreatic insufficiency Chronic Pancreatitis Type Chronic Obstructive Pancreatitis Inflammation, spasm and obstruction of the sphincter of Oddi Inflammation and sclerotic lesions occur at the head of the pancreas obstruction and backflow of secretion

Chronic Pancreatitis with pseudocysts Results Loss of exocrine function: Aqueous bicarbonate- neutralizes duodenal contents Pancreatic enzymes- what do they do? Enzyme secretion is reduced by 80% steatorrhea, what do the stools look like? Fat malabsorption wt loss and muscle wasting and edema r/t loss of albumin

Results Pancreatic endocrine dysfunction causes what disease? May also have pulmonary complications from edema and pancreatic ascites ARDS may develop Chronic pancreatitis is a major risk factor for pancreatic cancer Symptoms of Chronic Pancreatitis

Intense abdominal pain and tenderness Ascites What type of stools? Respiratory compromise Wt loss or gain? Jaundice What does the urine look like? Why? Signs of diabetes Elevated lipase and amylase Elevated bilirubin, alkaline phosphatase and glucose

Definitive dx- by biopsy to look for calcification Nursing Management Manage pain- how? Enzyme replacement- dietary supplements, pancrease, viokase, cotazyme, donnazyme- take before or during meals, take according to number of stools/day and wipe lips after Insulin therapy NPO or TPN for days, then what kind of diet? Histamine receptor blockers to decrease acid

Octreotide (Sandostatin) like somatostatin may be used for diarrhea to slow motility Health teaching Surgery is not an option, unless there is a cyst, obstruction or possible transplant for diabetes Diet and alcohol avoidance is stressed Medication compliance with insulin, pancreatic enzymes Skin care for irritation r/t steatorrhea What should the patient monitor?

Case Study 44 year old female admitted with abdominal pain, nausea and vomiting. She states that she has a lot of gas pain that wakes her up in the night. What do you suspect?

Case Study What are the symptoms of GB disease? What can precipitate it? What is the treatment? How can you prepare her for surgery? How do you decide between laparoscopic and open?

What needs to be done postop? Case Study What structures are located in the RUQ of the abdomen? Which of the above organs are palpable in the RUQ? Given the patients diagnosis, what lab values would be important to evaluate? List 4 preop preparations that to be done.

Case Study The patient undergoes a laproscopic cholecystectomy, why is a T-tube inserted? What type of postoperative care would be required? The patient is sent home with the T-tube, what care would be appropriate? What type of diet should they be on? Case Study The patient is medicated with Morphine and the pain

has decreased from 10-4 in 1 hour, what else could be done for his pain? What data charted in the assessment is consistent with common bile duct obstruction? The patient spikes a temp of 38.6, a CXR is ordered and the patient is started on an antibiotic, imipenem. What should be done before the antibiotic is started? Case Study She is ready for discharge

What type of teaching is needed? What should be avoided, what about care of the T-tube? Cholecystectomy

Removal of the Gallbladder Can be done open or laproscopic Signs are nausea, vomiting, abdominal pain Risk Factors: Fat, Female, Forty and Fertile lap cholecystectomy Lap Cholecystectomy T-tube

Post-operative Care Pain control- demerol or PCA NPO until bowel sounds return, then clear liquids to DAT Diet depends on what patient can tolerate T-tube may remain in for 1-6 weeks Monitor drainage, should be bile colored Less than 1000ml/day Never irrigate, aspirate or clamp a T-tube without an MD order

Disorders of the Liver Largest organ in the body and is located in the RUQ Large right lobe and smaller left lobe Made up of lobules Bile is made in hepatocytes, secreted into bile canaliculi Receives 1500 ml of blood/ min

Liver Functions 400 functions Storage: What types of vitamins and minerals? Protective: Kupfer cells, phagocytic, destroy bacteria, anemic

RBCs Detoxifies what? Metabolism: Makes proteins, for what? Breaks down amino acids to remove ammonia, converted to what? Synthesizes plasma proteins, albumin,

prothrombin and fibrinogen Stores and releases glycogen Breaks down and stores fatty acids and triglycerides Forms and secretes what substance? Liver Disorders

Cirrhosis/ Liver Failure Hepatitis Case Study 53 year old male admitted to the ED with abdominal pain, nausea and vomiting, weight loss. His abdomen is large and tender. His

skin is light yellow. He has a fruity odor to his breath. What do you suspect? Case Study What lab work should be done? What interventions would you perform and why? Your patient becomes belligerent after a few hours and wants to leave, what would you do?

What radiology studies may be done? Case Study His liver enzymes are extremely elevated and he is becoming confused. He is admitted to the floor. What symptoms are you likely to see in this patient? He starts to vomit blood, what does this mean and what may be done? What medications may be given to this

patient? Case Study He has improved and is now ready for discharge. What kind of teaching would this patient need? What should be done about rehab?

Cirrhosis Scarring of the liver, caused by a chronic, irreversible reaction to hepatic inflammation and necrosis Causes: #1 cause? #2 cause? Destruction of hepatocytes, tissue becomes nodular, block bile ducts and blood flow from fibrous connective tissue Liver begins enlarged and then shrinks

Cirrhosis Complications Compensated and Decompensated Cirrhosis Liver failure Portal hypertension, what is this? Ascites, why? Bleeding esophageal varices Coagulation defects, why? Jaundice, what causes this?

Portal systemic encephalopathy and coma Hepatorenal syndrome Bacterial peritonitis Liver Dysfunction PSE Esophageal Varices Jaundice

Bleeding Hepatorenal Syndrome Bacterial Peritonitis Ascites Portal Hypertension Increase in pressure within the portal vein Increased resistance or blockage in the flow of blood

through the portal vein Seeks collateral circulation Blood flows back into the spleen, causing splenomegaly What veins become dilated? Can lead to esphageal varices, caput medusa (what is that??) and hemorroids Ascites Accumulation of free fluid within the peritoneal cavity Increased hydrostatic pressure from the portal hypertension

causes fluid to leak into cavity Albumin accumulates in peritoneal fluid and this reduces the circulating proteins, this decreases serum colloid osmotic pressure and can lead to a decrease in what? Decrease in intravascular circulation causes renal vasoconstriction, triggers the renin-angiotensin system. This causes Na and water retention, which does what to fluid hydrostatic pressure and fluid volume?, where does the fluid accumulate? Ascites

Bleeding esophageal varices Blood backs up from liver into esophageal and gastric vessels Increased pressure, causes esophageal vessels to become fragile and distended Life threatening emergency, significant blood loss and this can lead to what? Bleeding is manifested as hematemesis and melena, what does that mean? Any activity that increases abdominal pressure can lead to

bleeding, such as what? Also, then to have portal hypertensive gastropathy, this leads to slow GI bleeds and cause chronic anemia Coagulation defects Decrease in the synthesis of bile, this prevents the absorption of fat-soluble vitamins and clotting factors are not produced What fat soluble vitamin is predominant in clotting? What lab values would be abnormal? Splenomegaly results from the backup of blood, this

destroys platelets and leads to thrombocytopenia, one of earliest signs of liver dysfunction Jaundice Hepatocellular disease and intrahepatic obstruction are the cause Liver cells can not excrete bilirubin, what are the liver cells called? Excessive circulating bilirubin Obstruction jaundice is from edema, fibrosis and scarring that block bile ducts

Excess bilirubin causes the skin to become yellow gold, sclera are yellow and skin is pruritic and frosty Portal system encephalopathy PSE or hepatic coma in later stages Altered level of consciousness, impaired thinking and neuromuscular disorders Can reverse the encephalopathy with early intervention Liver is unable to detoxify substances and ammonia

is most common cause Some encephalopathy may occur without elevated ammonia, may be other toxins Portal systemic encephalopathy Factors that may precipitate: High-protein diet Infections Hypovolemia Hypokalemia Constipation

GI bleeding, large protein load in intestines Drugs, such as hypnotics, opioids, sedatives, analgesics and diuretics Paracentesis or shunting of veins may also cause Why does protein increase encephalopathy?? Stages of encephalopathy Prodromal Personality changes, agitation, emotional lability, impaired thinking, fatigue, slurred speech, inability to concentrate Impending

Mental confusion, disoriented to person, place and time, asterixis (liver flap) how do you test for this? Stuporous Drowsy, but arousable, muscle twitching, hyperreflexia, abnormal EEG Comatose Unresponsive, 85% lead to death, obtunded, response to pain, no asterixis, positive babinski, muscle rigidity, fetor hepaticus, seizures, why seizures? Hepatorenal syndrome

Often cause of death Sudden decrease in urinary flow Elevated BUN and Creatinine levels and decreased urine sodium excretion Increased urine osmolarity, what is that? Why is there a decrease in fluid volume to the kidneys? Bacterial Peritonitis Occurs spontaneously Low concentrations of what type of proteins, that

protect against bacteria, cause this? Bacteria are from the bowel and reach the ascitic fluid when they are pulled through the bowel wall, what type of pressure would cause this? Symptoms are: fever, chills, abdominal pain and tenderness Diagnosis is made by culture of ascitic fluid and leukocyte count Causes of Cirrhosis Alcoholic hepatitis- if alcohol intake is stopped, liver

damage will reverse, if not, cellular necrosis continues. It may take years to develop Viral Hepatitis- C is most common, but B may also affect. It causes inflammation and cell damage Autoimmune hepatitis- autoantibodies Steatohepatitis- fatty liver fat and cholesterol deposits occur over time, cause is obesity and elevated lipids Drugs and toxins- medications, such as illegal drug use, chemotherapy, tylenol ! Biliary disease- primary biliary cirrhosis and primary sclerosing cholangitis

Metabolic- hematochromatosis, what is that?, Alphaantitrypsin deficiency and cystic fibrosis, why? Cirrhosis Patient Physical Manifestations

Fatigue Change in wt GI symptoms Abdominal pain and tenderness Pruritis

Jaundice and icterus (whats that?) Dry skin and rashes Petechiae and ecchymosis, why? Vascular lesions, spider angiomas on nose, checks, shoulders Dependent edema Physical manifestations

Ascites, can lead to disruption in what major function? Tested by fluid wave, what is that? How do you test for hepatomegaly? Why would you measure abdominal girth? Melena and fetor hepaticus may also be present, what does this mean? Amenorrhea, testicular atrophy and gynecomastia may also occur because of inactive hormones that are normally made in the liver

Fluid Wave Lab tests Elevated values are: AST ALT LDH Alkaline phosphatase Bilirubin in serum and urine Total protein

Serum globulin (immune response to liver disease) Ammonia Prothrombin time Decreased values are: Fecal urobilinogen Total protein (in chronic disease) Serum albumin

Other assessments CT scan, Ultrasound of liver Liver Biopsy, how is this done and what precautions should be taken? EGD- what does this mean and why would this be done, what are they looking for? Liver Biopsy Nursing Diagnoses

#1 is related to fluid volume, would it be excess or deficit fluid volume, what is it related to? What are two potential problems? What collaborative problems are these patients at risk for? (there are at least 7 or 8) Nursing Management of Excess Fluid Volume Diet Therapy Low Na diet, 500 to 2 gm/day IV and oral fluid is restricted to 1-1.5 L/day

Vitamin supplements, thiamine, folate may be needed Drug Therapy Diuretics, what are some? What should you monitor for? What electrolyte is affected by diuretics? Antibiotics to prevent bacterial peritonitis Management of Excess Fluid Volume Paracentesis MD inserts a catheter into the abdomen to remove and drain ascitic fluid

Should void first, HOB is elevated Should monitor vital signs and drain slowly, why? Cultures may be sent What blood product may be given prior to removing ascites fluid? Paracentesis Other measures

Comfort: Keep HOB elevated, use creams for pruritis Monitor lung sounds and give O2 if needed Monitor fluid and electrolyte levels Surgical: Peritoneovenous shunt- catheter and one way valve to let fluid flow from abdomen to superior vena cava, can have clots and infection Portacaval shunt- diverts blood from the liver to the kidney or

inferior vena cava TIPS- transjugular intrahepatic portal-systemic shunt, track is made between the portal vein, hepatic veins and systemic circulation. The shunts are kept open with stents that are inserted and this increases the systemic circulation and decreases the portal hypertension Peritoneal-venous Shunt TIPS

Nursing Outcomes for Excess Fluid Volume Name 8 desired nursing outcomes for a patient with excess fluid volume 1. 2. 3. 4. 5. 6. 7. 8.

Potential for Hemorrhage Goal is to prevent bleeding Drug therapy is to control HR and BP, this decreases the hepatic venous pressure gradient, may use a Beta Blocker to do both and keep the HR about 55/min Gastric Intubation- NGT with iced saline or water lavage to vasoconstrict ulcerations device.

Potential for Hemorrhage Balloon Tamponade- esophagogastric- Blakemore tube- it has 2 balloons, an esophageal and gastric, one balloon in esophagus to compress varices, one larger in stomach to anchor tube, and another lumen for suctioning. Inserted through the mouth, once in place, balloons are inflated and clamped. Traction may be performed by anchoring it to a helmet Potential for Hemorrhage Complications of the Blakemore tube are aspiration, the

balloons may decompress and become lodged in the back of the pharynx. Blood and gastric contents may also be aspirated. The stomach balloon should always be deflated first and then the esophageal. Blood transfusions may be needed and emergently, PRBCs and FFP Potential for Hemorrhage Endoscopic- Band Ligation- small O bands are placed around the base of the varices, octreotide may be given at the time to decrease bleeding and

secretions. Injection sclerotherapy may also be done to stop bleeding, a sclerosing agent is injected via endoscopy TIPS procedure or portal-systemic shunts may be needed What lab work should be monitored for these patients? Banded esophageal Varices Blakemore Tube

Portal Systemic Encephalopathy Ammonia is the probably cause, toxic to the brain Drug Therapy- Lactulose- high molecular wt disaccharide, it is thick and sticky with a sweet taste. It cleanses the GI tract and decreases the bacterial content, also creates and acid environment in the bowel and decreases the acid from 7-5, this keeps ammonia as an ion and pulls it into the colon. It may be given po or enema. Po is 20-30g q 4 hour. Monitor the number of stools and ammonia levels. It may cause cramping and often patients do not want to

take it. Portal-Systemic Encephalopathy Drug Therapy- Neomycin may also be used to cleanse the bowel and decrease protein breakdown, it can be given po or enema. Metronidazole (Flagyl) is also a bowel antibiotic with less renal side-effects Monitor the patient for neurologic changes, look for stupor, asterixis and fetor hepaticus Maintain patient safety

Patient Education Patient teaching should revolve around three main areas, what should be discussed under each? 1. Diet Therapy 2. Drug Therapy 3. Alcohol Abstinence Goal is to have a decrease in ascites, electrolytes WNL and no bleeding or PSE Hepatitis

Viral infection, can be acute or chronic, caused by one of five viruses, A-E, hepatitis F and G have been identified too Leads to inflammation of the liver cells Can also be caused by exposure to chemicals, toxins and medications Can be secondary to infections from Epstein-Barr, herpes, varicella and cytomegalovirus Hepatitis

Types of Hepatitis Hepatitis A HAV is an RNA virus Spread fecal-oral, contaminated water, shellfish and food contaminated by food handlers Incubation is 15-50 days Often the disease is mild and people dont know that they have it Can lead to more severe liver disease in compromised people

Types of Hepatitis Hepatitis B HBV, it is a particle of DNA that is surrounded by a core and surface antigen Spread by: Unprotected sex Sharing needles or needle sticks Blood transfusions, hemodialysis Maternal-fetal route

Symptoms occur in 25-180 days. They are: Anorexia, nausea, vomiting, fever, fatigue, RUQ pain, dark urine and light stool, joint pain and jaundice Can lead to cirrhosis and liver failure Often develop immunity and can become carriers Hepatitis C

HCV is a single strand RNA virus Transmitted blood to blood Spread by: IV drug needle sharing

Blood, blood products or transplants Needle stick injury with contaminated blood Tattoos and intranasal cocaine Not transmitted by casual contact Should not share razors, toothbrushes or pierced earrings Incubation is 21-140 days, average 7 weeks Most dont know they are infected until it becomes chronic Scarring leads to cirrhosis, can lead to liver cancer Many receive liver transplants Hepatitis D

HDV is a defective RNA virus that needs helper function of HBV Coinfects and needs HBV for replication Can be a superinfection and lead to a chronic infection Incubation is 14-56 days Spread is mostly IV blood transmission Hepatitis E HEV, single strand RNA virus Transmitted by fecal-oral route, similar to HAV

Waterborne epidemic in India, now in Asia, Africa, Middle East, Mexico and Central & South America Incubation of 15-64 days Incidence 250,000 people in the US develop HAV 200 million worldwide have HCV 3.9 million have HCV in the US and 3 million have chronic liver disease Chronic hepatitis is through to be inflammation of

the liver for > 6 months Usually the result of HCV or HBV Can lead to fulminant liver failure, which is lifethreatening, due to total failure of the organ Prevention What things can you tell a client to prevent the spread of hepatitis? (for both HAV and HBV/HCV) Which viruses have vaccines? If exposed to the virus, is there anything that can be taken?

Patient assessment Assess for: Abdominal pain

Jaundice Arthralgia Myalgia, why? Diarrhea Changes in stool and urine color Fever, lethargy Nausea/vomiting History of contamination Liver Biopsy- confirmatory

Labs: Liver enzymes- AST, ALT, alk phos, bilirubin all elevated Enzyme assays- antibodies to virus, anti-HAV, HBsAG (HBV surface antigen), anti HBcIgM (core antigen) Elisa for HCV and antiHCV Anti-HDV and HEV Usually present within 6

months Nursing Diagnoses What do you think are the most common nursing diagnoses for Hepatitis? 1. 2. 3. What interventions would be appropriate? Nursing Interventions

Drug Therapy Use medications sparingly to rest liver Antivirals, such as lamivudine (epivir-HBV) or Hepsera Interferon for HCV and HBV, SQ with ribavirin, take the combination for 24-48 weeks until negative HCV RNA level Home Care Education What type of home care education would be appropriate? Discuss disease with family, especially spread

Discuss community resources, chronic, long term disease Good handwashing, prevent spread of blood Measures to prevent the spread of infection to the patient Avoid alcohol Allow for rest periods Liver Transplantation

Assess patient both physically and psychologically prior to transplantation Contraindicated if: Severe cardiovascular or respiratory disease Active alcohol or drug use Metastatic disease Inability to follow treatment or lack of appropriate caregiver Most transplants are cadaver livers, but some are donors of single lobes. Usually done with children

Livers are obtained through the UNOS, United Network of Organ Sharing in cooperation with OPO, organ procurement organizations. In Jacksonville, we use Lifequest. There are presently 2300 people waiting for organ transplants within our area. Liver Transplantation Most common complications are graft rejection and infection Rejection can occur quickly or years out. Medications to prevent rejection are: Cell-cept, Prograf, Imuran, Sirolimus, prednisone and FK506 Signs of rejection are RUQ pain, fever, tachycardia, decreased

bile production and increased jaundice, elevated liver enzymes Liver Transplantation Infection Immunosuppressive therapy can cause rejection, plus they are very debilitated, immobile and have multiple lines Cytomegalovirus, mycobacterial and parasitic infections are most common Usually on many antibiotics

Other complications: Hemorrhage, hepatic artery thrombosis, pulmonary atelectasis, electrolyte imbalances- usually Ca, Mg and K, ARF Nursing Care Usually these patients are very ill, they may be in the ICU for many days, some are fast-tracked Return intubated, with a Swan line, arterial line and

have continuous cardiac outputs and SvO2 readings. Some are on CVVH (continuous veno-venous hemofiltration) for renal perfusion Need a lot of psychological support Liver transplantation liver transplant UNOS

Liver transplant video Y0Liver transplant surgery

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